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CO2 Regulation of Virulence Genes in Enteropathogenic Escherichia coli

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Mechanisms in the Pathogenesis of Enteric Diseases

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 412))

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Abstract

Enteropathogenic Escherichia coli (EPEC) are a heterogeneous group of bacteria implicated as a cause of severe persistent enteritis in infants (Robins-Browne 1987). The primary histopathological effect of EPEC infection is the so-called attaching and effacing (AE) lesion. This involves localised destruction of intestinal brush border microvilli and distortion of the apical enterocyte membrane into an actin-rich “pedestal” structure at the point of bacterial contact. Formation of AE lesions is a crucial aspect of the pathogenesis of EPEC. Loss of the absorptive surface of the gut mucosa by effacement of brush border microvilli contributes to disease by reducing NaCl uptake, while enterocyte death as a result of prolonged infection would inflict severe mucosal damage and lead to protracted diarrhoea.

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References

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© 1997 Springer Science+Business Media New York

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Haigh, R.D., Williams, P.H. (1997). CO2 Regulation of Virulence Genes in Enteropathogenic Escherichia coli . In: Paul, P.S., Francis, D.H., Benfield, D.A. (eds) Mechanisms in the Pathogenesis of Enteric Diseases. Advances in Experimental Medicine and Biology, vol 412. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1828-4_39

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  • DOI: https://doi.org/10.1007/978-1-4899-1828-4_39

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4899-1830-7

  • Online ISBN: 978-1-4899-1828-4

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