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Infection and Immunity, August 1999, p. 3733-3739, Vol. 67, No. 8
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Vibrio cholerae Intestinal Population
Dynamics in the Suckling Mouse Model of Infection
Michael J.
Angelichio,1
Jonathon
Spector,2
Matthew K.
Waldor,2,* and
Andrew
Camilli1,*
Department of Molecular Biology and
Microbiology, Tufts University School of
Medicine,1 and Division of Geographic
Medicine and Infectious Diseases, Tufts-New England Medical
Center,2 Boston, Massachusetts 02111
Received 19 January 1999/Returned for modification 29 March
1999/Accepted 27 April 1999
The suckling mouse has been used as a model to identify
Vibrio cholerae intestinal colonization factors for over
two decades, yet little is known about the location of recoverable
organisms along the gastrointestinal (GI) tract following intragastric
inoculation. In the present study, we determined the population
dynamics of wild-type and avirulent mutant derivatives of both
classical and El Tor biotype strains throughout the entire suckling
mouse GI tract at various times after intragastric inoculation.
Wild-type strains preferentially colonized the middle small bowel with
a sharp demarcation between more proximal segments which had
manyfold-fewer recoverable cells. Surprisingly, large and stable
populations of viable cells were also recovered from the cecum and
large bowel. Strains lacking toxin-coregulated pili (TCP
)
were cleared from the small bowel; however, an El Tor TCP
strain colonized the cecum and large bowel almost as well as the
wild-type strain. Strains lacking lipopolysaccharide O antigen (OA
) were efficiently cleared from the small bowel at
early times but then showed net growth for the remainder of the
infections. Moreover, large populations of the OA
strains
were maintained in the large bowel. These results show that for the El
Tor biotype neither TCP nor OA is required for colonization of the
suckling mouse large bowel. Finally, similar percent recoveries of
wild-type, TCP
, and OA
strains from the
small bowel at an early time after infection suggest that TCP and OA
are not required for strains of either biotype to resist bactericidal
mechanisms in the suckling mouse GI tract.
*
Corresponding author. Mailing address for Matthew K. Waldor: Division of Geographic Medicine and Infectious Diseases,
Tufts-New England Medical Center, 750 Washington St., Boston, MA 02111. Phone: (617) 636-7618. Fax: (617) 636-5292. E-mail:
matthew.waldor{at}es.nemc.org. Mailing address for Andrew
Camilli: Department of Molecular Biology and Microbiology, Tufts
University School of Medicine, 136 Harrison Ave., Boston, MA 02111. Phone: (617) 636-6653. Fax: (617) 636-0337. E-mail:
acamilli{at}opal.tufts.edu.
Infection and Immunity, August 1999, p. 3733-3739, Vol. 67, No. 8
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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