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Infection and Immunity, March 1999, p. 1201-1206, Vol. 67, No. 3
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Virulence of a spaP Mutant of
Streptococcus mutans in a Gnotobiotic Rat
Model
Paula J.
Crowley,1
L. Jeannine
Brady,1
Suzanne M.
Michalek,2 and
Arnold
S.
Bleiweis1,*
Department of Oral Biology, University of
Florida, Gainesville, Florida 32610,1 and
Department of Microbiology, University of Alabama at
Birmingham, Birmingham, Alabama 352942
Received 2 September 1998/Returned for modification 22 October
1998/Accepted 10 December 1998
Streptococcus mutans, the principal etiologic agent of
dental caries in humans, possesses a variety of virulence traits that enable it to establish itself in the oral cavity and initiate disease.
A 185-kDa cell surface-localized protein known variously as antigen
I/II, antigen B, PAc, and P1 has been postulated to be a virulence
factor in S. mutans. We showed previously that P1
expression is necessary for in vitro adherence of S. mutans to salivary agglutinin-coated hydroxyapatite as well as for fluid-phase aggregation. Since adherence of the organism is a necessary first step
toward colonization of the tooth surface, we sought to determine what
effect deletion of the gene for P1, spaP, has on the
colonization and subsequent cariogenicity of this organism in vivo.
Germ-free Fischer rats fed a diet containing 5% sucrose were infected
with either S. mutans NG8 or an NG8-derived
spaP mutant strain, PC3370, which had been constructed by
allelic exchange mutagenesis. At 1-week intervals for 6 weeks after
infection, total organisms recovered from mandibles were enumerated. At
week 6, caries lesions also were scored. A significantly lower number
of enamel and dentinal carious lesions was observed for the
mutant-infected rats, although there was no difference between parent
and mutant in the number of organisms recovered from teeth through 6 weeks postinfection. Coinfection of animals with both parent and
mutant strains resulted in an increasing predominance of the mutant
strain being recovered over time, suggesting that P1 is not a necessary
prerequisite for colonization. These data do, however, suggest a role
for P1 in the virulence of S. mutans, as reflected by a
decrease in the cariogenicity of bacteria lacking this surface protein.
*
Corresponding author. Mailing address: Department of
Oral Biology, University of Florida, P.O. Box 100424, Gainesville, FL 32610-0424. Phone: (352) 846-0787. Fax: (352) 392-7357. E-mail: bleiweis{at}dental.ufl.edu.
Infection and Immunity, March 1999, p. 1201-1206, Vol. 67, No. 3
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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