Abstract
The virulence of wild-type Pseudomonas aeruginosa PAO1 and that of a genetically defined algC mutant, PAO1 algC::tet, were compared in a burned-mouse model of infection. Unlike PAO1, PAO1 algC::tet was avirulent, grew less well in the eschar, and did not disseminate to the liver of challenged animals. We have previously shown that the P. aeruginosa algC gene is required for biosynthesis of alginate and lipopolysaccharide (M.J. Coyne, Jr., K.S. Russell, C.L. Coyle, and J.B. Goldberg, J. Bacteriol. 176:3500-3507, 1994). In order to determine whether the alginate or lipopolysaccharide (LPS) defect was responsible for the avirulence of this strain, we constructed a strain with a mutation in an alginate-specific gene, algD. PAO1-algD was virulent in the burned-mouse model, thus implicating the LPS defect in PAO1 algC::tet as the relevant alteration responsible for the avirulence of this strain.
MeSH Terms
Animals
Burns/complications
Female
Lipopolysaccharides/toxicity
Mice
Mutation
Phosphoglucomutase/physiology
Phosphotransferases (Phosphomutases)/physiology
Pseudomonas Infections/etiology
Pseudomonas aeruginosa/pathogenicity
Virulence
Chemicals
Lipopolysaccharides
Phosphotransferases (Phosphomutases)
Phosphoglucomutase
phosphomannomutase
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Goldberg J B
Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Coyne M J
Neely A N
Holder I A
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