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Pathogenic Mechanisms, Ecology, and Epidemiology

Experimental Shigella Infections in Laboratory Animals I. Antagonism by Human Normal Flora Components in Gnotobiotic Mice

Bruce R. Maier, David J. Hentges
Bruce R. Maier
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David J. Hentges
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ABSTRACT

Germfree mice were associated with selected species of human intestinal bacteria and then challenged with a streptomycin-resistant Shigella flexneri strain. Antagonism against Shigella was most pronounced in mice associated with Escherichia coli and least pronounced in mice associated with Bacteroides fragilis. A moderate degree of antagonism could be demonstrated in mice associated with either Streptococcus faecalis or Bifidobacterium adolescentis. Shigella persisted in the cecal contents of E. coli-associated mice at very low, stable levels. Shigella populations were reduced to levels below detection in the ceca of mice diassociated with E. coli and Bacteroides. Upon subsequent administration of streptomycin, Bacteroides disappeared from the ceca. The E. coli population was greatly reduced, and Shigella reappeared at very high population levels as an apparent recombinant which resembled E. coli biochemically. A streptomycin-resistant E. coli population subsequently emerged and became dominant in the ceca. Shigella concomitantly declined to levels below detection.

FOOTNOTES

  • ↵1 Presented in part at the Annual Meeting of the American Society for Microbiology, Minneapolis, 2-7 May, 1971.

  • ↵2 Taken from a dissertation presented to the Graduate School, University of Missouri, by B. R. Maier in partial fulfillment of requirements for the Ph.D. degree.

  • Copyright © 1972 American Society for Microbiology
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Experimental Shigella Infections in Laboratory Animals I. Antagonism by Human Normal Flora Components in Gnotobiotic Mice
Bruce R. Maier, David J. Hentges
Infection and Immunity Aug 1972, 6 (2) 168-173; DOI:

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Experimental Shigella Infections in Laboratory Animals I. Antagonism by Human Normal Flora Components in Gnotobiotic Mice
Bruce R. Maier, David J. Hentges
Infection and Immunity Aug 1972, 6 (2) 168-173; DOI:
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