Synergistic effect of mutations in invA and lpfC on the ability of Salmonella typhimurium to cause murine typhoid

• DOI: 10.1128/iai.65.6.2254-2259.1997
• Publication Date: 2020-01-06T19:17:34Z
• Authors: A J Bäumler; R M Tsolis; P J Valentine; T A Ficht; F Heffron
• Keywords: Pathogenicity island; Mesenteric lymph nodes; Salmonella infection; Intestinal mucosa

Penetration of the intestinal mucosa at areas Peyer's patches is an important first step for Salmonella typhimurium to produce lethal systemic disease in mice. However, mutations genes that are invasion result only moderately decreased virulence S. Here we report combining invA and lpfC, two necessary entry into patches, results a much stronger attenuation than inactivation either these alone. An lpfC mutant was 150-fold attenuated by oral route infection but fully virulent when intestine bypassed intraperitoneal challenge During mixed-infection experiments, showed strong defect colonizing mesenteric lymph nodes. These data suggest deactivate distinct pathways penetration colonization patches. While inv-mediated pathway widely distributed, lpf operon absent from many phylogenetic groups within genus Salmonella. To investigate how acquisition lpf-mediated mucosal contributed evolution virulence, studied relationship between presence pathogenicity mice 18 isolates representing 14 serotypes. Only strains possessing were able cause show both invA- lpfC-mediated perforation conserved mouse