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Altered Colonizing Ability for the Ceca of Broiler Chicks by Lipopolysaccharide-Deficient Mutants of Salmonella typhimurium

Stephen E. Craven
Avian Diseases
Vol. 38, No. 3 (Jul. - Sep., 1994), pp. 401-408
DOI: 10.2307/1592059
Stable URL: http://www.jstor.org/stable/1592059
Page Count: 8
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Altered Colonizing Ability for the Ceca of Broiler Chicks by Lipopolysaccharide-Deficient Mutants of Salmonella typhimurium
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Abstract

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 108 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. /// Se utilizó la cepa 3333/O de Salmonella typhimurium para evaluar el papel del lipopolisacárido bacteriano en la colonización intestinal de pollos de engorde por Salmonella. De esta cepa se aislaron mutantes TnPhoA sin lipopolisacárido. Las sensibilidades de las mutantes a los fagos lisos y rugosos y a los patrones electroforéticos en geles de poliacrilamida-sulfato dodecílico de sodio, indicaron un defecto en la cadena lateral del polisacárido de la molécula de lipopolisacárido. Se determinó la colonización mediante la administración oral de 108 organismos de cada cepa por pollo. Se administró la cepa original y las mutantes y se contaron las unidades formadoras de colonia en el ciego una a tres semanas después de la administración por sonda esofágica. Las unidades formadoras de colonia para las cepas deficientes en lipopolisacárido o no fueron detectadas, o fueron significantemente menores que las obtenidas en los pollos que recibieron la cepa original. En el bazo, la incidencia de la cepa original fue mayor que la de las cepas mutantes. Estudios in vitro con las mutantes deficientes en lipopolisacárido obtenidas en este estudio, lo mismo que con las obtenidas de la cepa LT2 de S. typhimurium, sugieren que los componentes de las cadenas laterales de los lipopolisacáridos pueden proteger la células bacterianas frente al moco intestinal del pollo. La capa de lipopolisacárido parece aumentar la persistencia de Salmonella en el tracto intestinal del ave.

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