Fates of acid-resistant and non-acid-resistant shiga toxin-producing escherichia coli strains in ruminant digestive contents in the absence and presence of probiotics
2010
Chaucheyras-Durand, Frédérique | Faqir, Fahima | Ameilbonne, Aurelie | Rozand, Christine | Martin, Christine | Unité de Microbiologie (MIC) ; Institut National de la Recherche Agronomique (INRA) | Qualité des Produits Animaux (QuaPA) ; Institut National de la Recherche Agronomique (INRA) | Lallemand S.A.S. | Unite de Microbiologie Alimentaire et Previsionnelle ; Ecole Nationale Vétérinaire de Lyon (ENVL)
International audience
显示更多 [+] 显示较少 [-]英语. Healthy ruminants are the main reservoir of Shiga toxin-producing Escherichia coli (STEC). During their transit through the ruminant gastrointestinal tract, STEC encounters a number of acidic environments. As all STEC strains are not equally resistant to acidic conditions, the purpose of this study was to investigate whether acid resistance confers an ecological advantage to STEC strains in ruminant digestive contents and whether acid resistance mechanisms are induced in the rumen compartment. We found that acid-resistant STEC survived at higher rates during prolonged incubation in rumen fluid than acid-sensitive STEC and that they resisted the highly acidic conditions of the abomasum fluid, whereas acid-sensitive strains were killed. However, transit through the rumen contents allowed acid-sensitive strains to survive in the abomasum fluid at levels similar to those of acid-resistant STEC. The acid resistance status of the strains had little influence on STEC growth in jejunal and cecal contents. Supplementation with the probiotic Saccharomyces cerevisiae CNCM I-1077 or Lactobacillus acidophilus BT-1386 led to killing of all of the strains tested during prolonged incubation in the rumen contents, but it did not have any influence in the other digestive compartments. In addition, S. cerevisiae did not limit the induction of acid resistance in the rumen fluid. Our results indicate that the rumen compartment could be a relevant target for intervention strategies that could both limit STEC survival and eliminate induction of acid resistance mechanisms in order to decrease the number of viable STEC cells reaching the hindgut and thus STEC shedding and food contamination.
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