Enteric bacteria possess multiple fimbriae, many of which play critical rol
es in attachment to epithelial cell surfaces. SEF14 fimbriae are only found
in Salmonella enterica serovar Enteritidis (S. enteritidis) and closely re
lated serovars, suggesting that SEF14 fimbriae may affect serovar-specific
virulence traits. Despite evidence that SEF14 fimbriae are expressed by 5.
enteritidis in vivo, previous studies showed that SEF14 fimbriae do not med
iate adhesion to the intestinal epithelium. Therefore, we tested whether SE
F14 fimbriae are required for virulence at a stage in infection after the b
acteria have passed the intestinal barrier. Polar mutations that disrupt th
e entire sef operon decreased virulence in mice more than 1,000-fold. Nonpo
lar mutations that disrupted sefA (encoding the major structural subunit) d
id not affect virulence, but mutations that disrupted sefD (encoding the pu
tative adhesion subunit) resulted in a severe virulence defect. The results
indicate that the putative SEF14 adhesion subunit is specifically required
for a stage of the infection subsequent to transit across the intestinal b
arrier. Therefore, we tested whether SefD is required for uptake or surviva
l in macrophages. The majority of wild-type bacteria were detected inside m
acrophages soon after i.p. infection, but the sefD mutants were not readily
internalized by peritoneal macrophages, These results indicate that the po
tential SEF14 adhesion subunit is essential for efficient uptake or surviva
l of 5. enteritidis in macrophages. This report describes a role of fimbria
e in intracellular infection, and indicates that fimbriae may be required f
or systemic infections at stages beyond the initial colonization of host ep
ithelial surfaces.