Complete Lipopolysaccharide ofIs Required for Full Virulence in the Intraperitoneally Challenged Atlantic Salmon,, Model.

Abstract

Bacterial cell envelopes play a critical role in host-pathogen interactions. Macromolecular components of these structures have been closely linked to the virulence of pathogens.is a relevant salmonid pathogen with a worldwide distribution. This bacterium is the etiological agent of piscirickettsiosis, a septicemic disease that causes a high economic burden, especially for the Chilean salmon farming industry. Althoughhas been discovered long ago, its pathogenicity and virulence mechanisms are not completely understood. In this work, we present a genetic approach for producing in-frame deletion mutants on genes related to the biosynthesis of membrane-associated polysaccharides. We provide a detailedphenotype description of knock-out mutants onandgenes, which encode predicted lipopolysaccharide (LPS) flippase and undecaprenyl-phosphate glucose phosphotransferase enzymes, respectively. We exhibit evidence that themutant strain carries a defect in the probably most external LPS moiety, while themutant proved to be highly susceptible to the bactericidal action of serum but retained the ability of biofilm production. Beyond that, we demonstrate that the deletion of, but not, impairs the virulence ofin an intraperitoneally infected Atlantic salmon,, model of piscirickettsiosis. Our findings support a role for LPS in the virulence ofduring the onset of piscirickettsiosis.