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The eae gene of Citrobacter freundii biotype 4280 is necessary for colonization in transmissible murine colonic

D B Schauer1, S Falkow

  • 1Department of Microbiology and Immunology, Stanford University School of Medicine, California 94305-5402.

Infection and Immunity
|November 1, 1993
PubMed

Insights

Citrobacter freundii causes murine colonic hyperplasia by producing attaching and effacing lesions. The chromosomal eae gene is essential for colonization, but a specific plasmid is not required for hyperplasia.

Area of Science:

  • Microbiology
  • Gastroenterology
  • Pathogenesis

Background:

  • Transmissible murine colonic hyperplasia is a condition affecting laboratory mice.
  • It involves the proliferation of stem cells in the colon's mucosa.
  • Citrobacter freundii biotype 4280 is identified as the causative agent.

Purpose of the Study:

  • To investigate the role of specific genes and plasmids in Citrobacter freundii-induced murine colonic hyperplasia.
  • To understand the mechanism by which C. freundii colonizes the mouse colon and causes disease.

Main Methods:

  • Mutational analysis of the chromosomal eae gene in C. freundii.
  • Comparison of wild-type C. freundii with bacteria cured of a 65-kb plasmid.
  • Assessment of colonic colonization and hyperplasia induction in laboratory mice.

Main Results:

  • The chromosomal eae gene of C. freundii biotype 4280 is essential for colonic colonization.
  • Bacteria lacking a specific 65-kb plasmid were still capable of colonizing the colon.
  • The 65-kb plasmid was not required for the induction of colonic hyperplasia.

Conclusions:

  • The eae gene plays a critical role in the pathogenesis of murine colonic hyperplasia by C. freundii.
  • A specific 65-kb plasmid in C. freundii biotype 4280 is not essential for causing colonic hyperplasia or colonization.

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