Streptococcus mutans, the principal etiologic agent of dental caries in hum
ans, possesses a variety of virulence traits that enable it to establish it
self in the oral cavity and initiate disease. A 185-kDa cell surface-locali
zed protein known variously as antigen I/II, antigen. B, PAc, and P1 has be
en postulated to be a virulence factor in S. mutans, We showed previously t
hat pi expression is necessary for in vitro adherence of S. mutans to saliv
ary agglutinin-coated hydroxyapatite as well as for fluid-phase aggregation
. Since adherence of the organism is a necessary first step toward coloniza
tion of the tooth surface, we sought to determine what effect deletion of t
he 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% s
ucrose were infected with either S. mutans NG8 or an NGS-derived spaP mutan
t strain, PC3370, which had been constructed by allelic exchange mutagenesi
s, At 1-week intervals for 6 weeks after infection, total organisms recover
ed from mandibles were enumerated. At week 6, caries lesions also were scor
ed. A significantly lower number of enamel and dentinal carious lesions was
observed for the mutant-infected rats, although there was no difference be
tween parent and mutant in the number of organisms recovered from teeth thr
ough 6 weeks postinfection, Coinfection of animals with both parent and mut
ant strains resulted in an increasing predominance of the mutant strain bei
ng recovered over time, suggesting that P1 is not a necessary prerequisite
for colonization, These data do, however, suggest a role for pi in the viru
lence of S. mutans, as reflected by a decrease in the cariogenicity of bact
eria lacking this surface protein.