Altered colonizing ability for the ceca of broiler chicks by lipopolysaccharide-deficient mutants of Salmonella typhimurium.
Salmonella typhimurium strain 3333/O was used to assess the role of bacterial lipopolysaccharide (LPS) in intestinal colonization of broiler chicks by salmonellae. LPS-defective TnPhoA mutants of this strain were isolated. The sensitivities of the mutants to smooth and rough phages and LPS banding patterns in sodium dodecyl sulfate-polyacrylamide gel electrophoresis indicated a defect in the polysaccharide side chain of the LPS molecule. Colonization was determined by orally administering 10(8) cells each of the wild-type and/or the mutant strains per chick and counting the colony-forming units (CFU) from the ceca 1 to 3 weeks after gavage. CFU of chicks given the LPS-deficient strains either were not detected or were significantly lower than the CFU from chicks given the wild-type strain. The incidence of the wild-type strain in spleens was higher than incidence of the mutant strains. In vitro binding studies with LPS-deficient mutants derived in this study and from S. typhimurium LT2 suggest that LPS side-chain components may shield the bacterial cell from entrapment in the chicken mucus. The LPS layer appears to enhance persistence of Salmonella in the avian intestinal tract.
Craven
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Poultry Microbiological Safety Research Unit, R. B. Russell Agricultural Research Center, U.S. Department of Agriculture, Athens, Georgia 30613.
D000818:Animals; D001422:Bacterial Adhesion / Q000235:genetics / Q000502:physiology; D002432:Cecum / Q000382:microbiology*; D002645:Chickens / Q000382:microbiology*; D066298:In Vitro Techniques; D008070:Lipopolysaccharides / Q000633:toxicity*; D009093:Mucus / Q000382:microbiology; D009154:Mutation; D012486:Salmonella typhimurium / Q000235:genetics / Q000254:growth & development* / Q000472:pathogenicity; D014774:Virulence / Q000235:genetics / Q000502:physiology
D008070:Lipopolysaccharides