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.
Poultry Microbiological Safety Research Unit, R. B. Russell Agricultural Research Center, U.S. Department of Agriculture, Athens, Georgia 30613.
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Craven
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