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Applied and Environmental Microbiology, April 2000, p. 1759-1763, Vol. 66, No. 4
Department of Veterinary PathoBiology,
University of Minnesota, St. Paul, Minnesota
551081; Department of Microbiology and
Immunology, University of South Alabama, Mobile, Alabama
366882; and Department of Laboratory
Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota
554553
Received 15 June 1999/Accepted 3 January 2000
Very little is known about the contribution of surface appendages
of Salmonella enterica serovar Enteritidis to pathogenesis in chickens. This study was designed to clarify the role of SEF14, SEF17, and SEF21 fimbriae in serovar Enteritidis pathogenesis. Stable,
single, defined sefA (SEF14), agfA (SEF17), and
fimA (SEF21) insertionally inactivated fimbrial gene
mutants of serovar Enteritidis were constructed. All mutant strains
invaded Caco-2 and HT-29 enterocytes at levels similar to that of the
wild type. Both mutant and wild-type strains were ingested equally well
by chicken macrophage cell lines HD11 and MQ-NCSU. There were no
significant differences in the abilities of these strains to colonize
chicken ceca. The SEF14
0099-2240/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Pathogenic Role of SEF14, SEF17, and SEF21 Fimbriae
in Salmonella enterica Serovar Enteritidis Infection
of Chickens

strain was isolated in lower
numbers from the livers of infected chickens and was cleared from the
spleens faster than other strains. No significant differences in fecal
shedding of these strains were observed.
*
Corresponding author. Mailing address: Department of
Veterinary PathoBiology, 1971 Commonwealth Ave., University of
Minnesota, St. Paul, MN 55108. Phone: (612) 625-9704. Fax: (612)
625-5203. E-mail: nagar001{at}maroon.tc.umn.edu.
Present address: Department of Microbiology and Immunology, Emory
University, Atlanta, GA 30322.
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